Regulation of the metastatic process by E-selectin and stress-activated protein kinase-2/p38.
Ann N Y Acad Sci
; 973: 562-72, 2002 Nov.
Article
em En
| MEDLINE
| ID: mdl-12485930
ABSTRACT
The formation of metastasis is a dreadful complication of cancer that is associated with a poor prognosis. Several clinical observations and experimental findings indicate that the metastatic process is nonrandom and involves a sequence of multistep events that may all be targeted for therapy. This includes angiogenesis of the primary neoplasm, release of malignant cells from this neoplasm, entry of cancer cells into the blood circulation, interaction of cancer cells with vascular endothelial cells in distant organs, and growth of blood-borne cancer cells locally in the vessels or distally following extravasation. Our working hypothesis is that metastatic cancer cells exploit the mechanisms of the inflammation process to successfully migrate into distant organs. This implies a pivotal role for specific adhesive interactions between cancer cells and vascular endothelial cells and activation of migratory pathways in the cancer cells. We review here the roles played by the endothelial adhesive molecule E-selectin and by the motogenic stress-activated protein kinase-2 (SAPK2/p38) pathway of cancer cells in modulating transendothelial migration of cancer cells.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Selectina E
/
Proteínas Quinases Ativadas por Mitógeno
/
Metástase Neoplásica
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Ann N Y Acad Sci
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Canadá